AI Article Synopsis
- Carbon black nanoparticles (CBNPs) can cause DNA damage in human bronchial epithelial cells, but how this leads to cancer is not fully understood.
- Researchers created an in vitro model to study this and found that long-term exposure to CBNPs resulted in tumor-like transformations and persistent DNA damage.
- They discovered that a specific circular RNA, circ_0025373, helps protect against DNA damage by regulating a key DNA repair gene, MSH2, which could provide new insights into lung cancer treatment and the risks associated with CBNPs.
Article Abstract
Carbon black nanoparticles (CBNPs) have been demonstrated to induce DNA damage in epithelial cells. However, the potential of the damage to initiate carcinogenesis and the underlying mechanism remain poorly understood. Therefore, we constructed an in vitro model of malignant transformation of human bronchial epithelial cells (16HBE-T) by treating 40 μg/mL CBNPs for 120 passages. We observed tumor-like transformation and sustained DNA damage. Using transcriptome sequencing and RIP-seq, we identified the overexpression of the critical DNA mismatch repair genes MutS homolog 2 (MSH2) and its related circular RNA, circ_0025373, in the 16HBE-T cells. Mechanistically, circ_0025373 was found to inhibit DNA damage by binding to MSH2, thereby modifying its expression and influencing its nuclear and cytoplasmic distribution, which lead to inhibition of CBNP-induced malignant transformation of human bronchial epithelial cells. Our findings provide novel evidence on the carcinogenicity of CBNPs, and offer biological insights into the potential epigenetic regulation and potential therapeutic targets for lung carcinogenesis.
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| http://dx.doi.org/10.1016/j.envint.2024.109001 | DOI Listing |
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